Short-term Shock Research Articles

Performance response and recovery of temporal and spatial phase separated process for nutrients removal in short-term shock loadings

This study was conducted to evaluate the stability and performance response under short-term hydraulic and organic shock load conditions in temporal and spatial phase separated process. The overall removals of BOD, TN, and TP declined slightly despite the hydraulic shock loading, and rapid recovery could be observed again after four cycles of 16h. It seems that rapid recovery may be achieved by the unique characteristics of the system operated in a fed-batch manner. The effect of shock load on nitrogen removal due to increment of flow rate was higher than that of phosphorus, because of the insufficient reaction time for the nitrification and denitrification. After the organic shock, however, recovery time for phosphorus removal was needed rather than that of organics and nitrogen, because the overload to micro organisms related to the phosphorus release is attained by short-term organic shock loading.

End of the Century pCO2 Levels Do Not Impact Calcification in Mediterranean Cold-Water Corals

Ocean acidification caused by anthropogenic uptake of CO2 is perceived to be a major threat to calcifying organisms. Cold-water corals were thought to be strongly affected by a decrease in ocean pH due to their abundance in deep and cold waters which, in contrast to tropical coral reef waters, will soon become corrosive to calcium carbonate. Calcification rates of two Mediterranean cold-water coral species, Lophelia pertusa and Madrepora oculata, were measured under variable partial pressure of CO2 (pCO2) that ranged between 380 µatm for present-day conditions and 930 µatm for the end of the century. The present study addressed both short- and long-term responses by repeatedly determining calcification rates on the same specimens over a period of 9 months. Besides studying the direct, short-term response to elevated pCO2 levels, the study aimed to elucidate the potential for acclimation of calcification of cold-water corals to ocean acidification. Net calcification of both species was unaffected by the levels of pCO2 investigated and revealed no short-term shock and, therefore, no long-term acclimation in calcification to changes in the carbonate chemistry. There was an effect of time during repeated experiments with increasing net calcification rates for both species, however, as this pattern was found in all treatments, there is no indication that acclimation of calcification to ocean acidification occurred. The use of controls (initial and ambient net calcification rates) indicated that this increase was not caused by acclimation in calcification response to higher pCO2. An extrapolation of these data suggests that calcification of these two cold-water corals will not be affected by the pCO2 level projected at the end of the century.

Interaction of the synthetic peptide octarphin with rat adrenal cortex membranes

The synthetic peptide octarphin (TPLVTLFK, fragment 12-19 of β-endorphin), a selective agonist of the non-opioid β-endorphin receptor, was labeled with tritium yielding specific activity of 28 Ci/mmol. The binding of [3H]octarphin to rat adrenal cortex membranes was studied under normal conditions as well as after cold and heat shocks. It was found that under normal conditions [(3)H]octarphin specifically binds to the membranes with high affinity: K(d1) = 36.3 ± 2.5 nM, B(max1) = 41.0 ± 3.8 pmol/mg protein. The specific binding of [(3)H]octarphin to the membranes was inhibited by unlabeled β-endorphin (K(i) = 33.9 ± 3.6 nM) and the agonist of the non-opioid receptor decapeptide immunorphin (K(i) = 36.8 ± 3.3 nM). Unlabeled naloxone, [Leu(5)]- and [Met(5)]enkephalins, α- and γ-endorphins, and corticotropin were inactive (K(i) > 1 µM). Both cold and heat shocks decreased the binding affinity: K(d2) = 55.6 ± 4.2 nM and K(d3) = 122.7 ± 5.6 nM, respectively. In both cases, the maximal binding capacity of the receptor did not change. Thus, even a short-term thermal shock significantly affects the sensitivity of the non-opioid β-endorphin receptor of adrenal cortex membranes.

Cellular distribution of NKCC2 in the gastric mucosa and its response to short-term osmotic shock

The Na(+)-K(+)-2Cl(-) cotransporter-2 (NKCC2) has long been recognized as a "kidney-specific" transporter and is important in salt reabsorption. NKCC2 has been found in the gastric mucosa; however, its cellular distribution and function remain obscure. The present study characterized the distribution pattern of NKCC2 in mammalian gastric mucosa and investigated its response to osmotic challenge. Reverse transcription with the polymerase chain reaction, Western blot and immunofluorescence were used to determine NKCC2 expression and localization. The effect of osmotic shock on NKCC2 expression was studied in isolated gastric mucosa with variable osmolarity treatment. Results from all of the above studies were compared with those of NKCC1. Our data indicated that NKCC1 and NKCC2 were expressed in the gastric mucosa of rat, mouse and human. The mRNA transcripts and proteins for NKCC1 and NKCC2 were broadly expressed in the rat gastric mucosa. In rat and mouse, NKCC1 was largely confined to the lower part of the oxyntic and pyloric gland areas, whereas NKCC2 extended throughout the gastric glands. NKCC1 immunoreactivity was strongly expressed in the parietal and chief cells but was weaker in the mucous cells. NKCC2 was abundantly located in the parietal and mucous cells but faintly distributed in the chief cells. Hypertonic treatment increased the protein level of NKCC1 and caused evident membrane translocation. In contrast, NKCC2 was significantly downregulated and no obvious membrane translocation was observed. Thus, NKCC2 displayed a more ubiquitous distribution in the gastric mucosa and might work coordinately with NKCC1 to maintain cell volume homeostasis under hypertonic conditions.

Resistance capability of microaerobic granular sludge for pentachlorophenol (PCP) degradation subjected to pH shock

The resistance capability to pH shock of microaerobic granular sludge for pentachlorophenol (PCP) degradation was studied. The results show that it had little effect on the system under short-term shock, and the system returned to normal state immediately，while large adverse effect occurred under long-term shock, and the system required long time to recover. The content of extracellular polymers (ECPs) including proteins (PN) and polysaccharides (PS) decreased significantly, as well as the ratio of proteins and polysaccharides for 8 days pH shock, and there was an increase in sludge volumetric index (SVI) values of sludge and a decrease in settling velocity. Compared with the normal pH, it was found that the number of bacillus in microorganisms reduced for pH shock, and recession-type cells occurred by being observed with scanning electron microscope, especially at pH 6.0 and 9.0 there was a more serious decline in the treatment effect and deterioration in the physicochemical properties of granular sludge.

Impact of International Financial Shocks on Small Open Economies: The Case of Four ASEAN Countries

A more integrated global financial system has implications on the economic volatility of small open economies. This paper simulates the impact of a short term shock originating from the global financial system on small open economies in the Association of Southeast Asian Nations (ASEAN). The simulation is conducted by means of empirically estimated small open economy dynamic stochastic general equilibrium models for Indonesia, Malaysia, the Philippines, and Thailand. The analysis highlights similarities and differences of the impact of a pure international financial shock on aggregate domestic price inflation and on output gap for each of the four ASEAN countries. It suggests that the impact of such shock on the sampled economies tends to be relatively small but long lasting, hence placing challenges on the task of managing economic volatility in these economies.

248 INVOLVEMENT OF THE SPHINGOLIPID, CERAMIDE, IN HEAT SHOCK-INDUCED APOPTOSIS IN BOVINE OOCYTE

Programmed cell death through the sphingomyelin pathway has been suggested to underlie the mechanism by which heat shock disturbs oocyte developmental competence. Serial experiments were performed to characterize the role of the sphingolipid ceramide in heat-shock-induced apoptosis, and to determine whether ceramide formation could be regulated. In all experiments, bovine cumulus–oocyte complexes (COC) were aspirated from ovaries collected at the abattoir. Cumulus–oocyte complexes were matured (22 h, 38.5°C, 5% CO2), in vitro fertilized (18 h, 38.5°C, 5% CO2), and cultured for 8 days (KSOM; 38.5°C, 5% CO2, 5% O2). In the first experiment, COC were matured at 38.5°C (n = 673) or 41°C (heat shock; n = 718). Exposure of COC to heat shock during maturation reduced cleavage (92.3 v. 84.2%; P < 0.05) and blastocyst formation rates (24.1 v. 14.6%; P < 0.05) relative to the control groups. In the second experiment, COC (n = 563) were exposed to either long-term (22 h) or short-term (0.5 to 3.5 h) heat shock during maturation. An Annexin V-FITC assay (Bender) was used to identify the turnover of phosphatidylserine, one of the features of early-stage apoptosis. In addition, a subgroup of matured oocytes (n = 384) were denuded and fixed in 2% paraformaldehyde, followed by immunofluorescent staining using anti-ceramide (Alexis) to detect ceramide levels and counterstaining with Hoechst (Sigma). Immunofluorescent staining showed no difference in endogenous ceramide levels between groups. Similarly, annexin expression did not differ between groups at the end of the maturation but was higher (P < 0.05) in oocytes exposed to short-term heat shock than in those subjected to long-term heat shock, suggesting that early features of apoptosis should be examined at a specific time of heat exposure. Another experiment was performed to examine the effect of ceramide on oocyte developmental competence. Cumulus–oocyte complexes (n = 1185) were matured with or without 10, 30, and 50 μm C2-ceramide (Sigma). An Annexin V-FITC assay was used with a subgroup of oocytes (n = 137) that were matured with or without 50 μm C2-ceramide for 2 h. To examine the major pathway of ceramide generation, heat-shocked COC were matured with or without 5 μm fumonisin B1 (FB1; Sigma), a specific inhibitor of dihydroceramide synthase (i.e. de novo formation) and ceramide synthase (i.e. salvage pathway), or with 5 μm desipramine hydrochloride (DH; Sigma), a specific inhibitor of the acid sphingomyelinase (i.e. hydrolysis). Results revealed that maturation in 50 μm C2-ceramide increased (P < 0.05) annexin expression in association with reducing cleavage rate and blastocyst formation (P < 0.05). Although not significant, maturation with FB1 moderated the heat-shock effect on oocyte developmental competence. Similarly, 5 μm DH increased the blastocyst formation rate for heat-shocked oocytes from a level of 17% to the control level (22.5%). In summary, ceramide appears to play an important role in heat-shock-induced apoptosis because blocking ceramide formation alleviated its deleterious effect. Research was supported in part by USDA Grant 2007-35203 and BARD Grant 3986-07

Akt Depletion Is an Important Determinant of L929 Cell Death following Heat Stress

Exposure of mammalian cells to heat stress causes impairment of numerous physiological functions and activates a number of signaling pathways. Some of these pathways, such as induction of heat-shock proteins and activation of Akt, enhance the ability of cells to survive heat stress. On the other hand, heat stress can trigger cell-death signaling via activation of the stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/Jnk). Recently, it has been shown that kinases activated by heat stress can regulate synthesis and functioning of the molecular chaperones, and these chaperones modulate the activity of the cell death and survival pathways. We have found that Akt plays a central role in determining the fate of L929 fibroblast cells exposed to heat stress. In our experiments heat stress causes Akt depletion and L929 cells to undergo cell death. Heat-shock protein 70 (Hsp70) is known to prevent stress-induced cell death by interfering with the SAPK/Jnk signaling pathway. In our study, there is a very high level of induction of Hsp70, yet this is not sufficient to rescue Akt depletion and L929 from cell death. The Akt depletion is specific, since actin protein level does not change during the heat stress. Moreover, our studies show that L929 cells can recover from a short-term heat shock, whereby, Akt level is returned to normal following recovery from heat shock. Therefore, it appears that the fate of the prolonged heat-stressed fibroblast cells is determined by Akt level, and that return of Akt protein level to normal prevents cell death.

Treatment of renal calculi by lithotripsy: minimizing short-term shock wave induced renal damage by using antioxidants

Treatment with extracorporeal shock wave lithotripsy (ESWL), the preferred method of treating kidney stones <3 cm in size, has been shown to induce silent and often self-limiting acute and chronic lesions in the kidneys and adjacent organs. We conducted a randomized clinical trial to determine whether ESWL produces ischaemia and reperfusion injury in the kidneys and whether oral administration of antioxidants reduces the degree of short-term renal injury in patients treated with ESWL. The study included 120 patients with renal stones (1-3 cm in size) treated with ESWL. The patients were divided into three groups--patients in group A (n=39) served as a control group and were not given any antioxidants; patients in group B (n=41) were given two capsules of antioxidants "Nature Made R: " 2 h before ESWL, and 2 and 8 h after ESWL; and patients in group C (n=40) were given two capsules of the antioxidants 2 and 8 h after ESWL. Double 'J' stents were inserted in patients before treatment with ESWL. Blood and urine samples were obtained from all patients just before the start of treatment with ESWL, and at 2 and 24 h and on 7th and 28th day after ESWL. Serum levels of malondialdehyde (MDA), alpha-tocopherol, cholesterol, albumin and ascorbic acid, and alpha-tocopherol/cholesterol ratio were determined. Urinary levels of albumin and beta(2) microglobulin were also determined as measures of renal tubular injury. At 24 h after ESWL, patients given antioxidants (groups B + C) had significantly reduced mean serum concentration of MDA (P<0.001); higher levels of serum ascorbic acid (P<0.001) and serum albumin (P<0.001); lower alpha-tocopherol/cholesterol ratio, lower urinary albumin and beta(2 )microglobulin levels compared with patients who did not receive antioxidants (group A). These findings suggest that treatment with ESWL generates free radicals through ischaemic/reperfusion injury mechanism, and that oral administration of antioxidant may protect these patients from short term renal injury caused by ESWL.

Organic and Hydraulic Shock Loadings on a Biological Aerated Filter

The performance of a biological aerated filter (BAF) during short-term (60 min) organic and hydraulic shock loads was investigated. The BAF used for the present experiment was not capable of absorbing high peak organic shock loads when the organic loads were increased from a normal load of 1.2–1.4 kg soluble chemical oxygen demand (sCOD) m−3 d−1 to shock loads between 5.1– 7.3 kg sCOD m−3 d−1, based on empty bed volumes. Nevertheless, the effect on the biomass was limited as normal performance resumed very quickly. Increases in the hydraulic velocity from 0.7–1.0 m h−1 to 1.5–2.9 m h−1 had little effect on BAF performance in terms of soluble COD removal. Yet, sCOD effluent concentrations of <55 mg l−1 (~22 mg l−1 biochemical oxygen demand) were always achieved. The recovery of the reactor in both cases was fast, resuming normal performance within 60 min after the application of the shock load.

Expression and intracellular localization of heat shock proteins in multidrug resistance of a cisplatin resistant human ovarian cancer cell line.

TYK-R10 is a cisplatin resistant human ovarian carcinoma cell line and showed a cross resistance to various anti-cancer drugs including adriamycin (ADR), vincristine (VCR) and etoposide, despite a lack of multidrug phenotype. Under normal conditions, various heat shock proteins (HSPs) were expressed in TYK-R10 but not in parental line (TYK-nu). Non-lethal short-term heat shock treatment induced a high tolerance for cisplatin and VCR in TYK-R10 and ADR, and VCR in TYK-nu. This treatment induced and/or enhanced the expression of various types of HSPs in various intracellular localizations in both TYK-R10 and TYK-nu, with minor differences. These findings indicate that combined expression and intracellular localization of HSPs may play an important role in drug resistance of TYK-R10.